Editing Post-traumatic stress disorder (section)

=== Neuroanatomy ===
[[File:PTSD stress brain.gif|thumb|220px|Regions of the brain associated with stress and post-traumatic stress disorder<ref>{{cite web |url=http://www.nimh.nih.gov/health/publications/post-traumatic-stress-disorder-research-fact-sheet/index.shtml |title=NIMH · Post Traumatic Stress Disorder Research Fact Sheet |work=[[National Institutes of Health]] |access-date=2014-01-29 |url-status=live |archive-url=https://web.archive.org/web/20140123205303/http://www.nimh.nih.gov/health/publications/post-traumatic-stress-disorder-research-fact-sheet/index.shtml |archive-date=2014-01-23}}</ref>]]

A [[meta-analysis]] of structural MRI studies found an association with reduced total brain volume, intracranial volume, and volumes of the [[hippocampus]], [[insula cortex]], and [[anterior cingulate]].<ref>{{cite journal |vauthors=Bromis K, Calem M, Reinders AA, Williams SC, Kempton MJ |title=Meta-Analysis of 89 Structural MRI Studies in Posttraumatic Stress Disorder and Comparison With Major Depressive Disorder |journal=The American Journal of Psychiatry |volume=175 |issue=10 |pages=989–998 |date=July 2018 |pmid=30021460 |pmc=6169727 |doi=10.1176/appi.ajp.2018.17111199}}</ref> Much of this research stems from PTSD in those exposed to the Vietnam War.<ref>{{Cite book |vauthors=Liberzon I, Sripada CS |volume=167 |pages=151–69 |date=2008 |pmid=18037013 |doi=10.1016/S0079-6123(07)67011-3 |isbn=978-0-444-53140-7 |series=Progress in Brain Research |title=Stress Hormones and Post Traumatic Stress Disorder Basic Studies and Clinical Perspectives |chapter=The functional neuroanatomy of PTSD: A critical review}}</ref><ref>{{cite journal |vauthors=Hughes KC, Shin LM |title=Functional neuroimaging studies of post-traumatic stress disorder |journal=Expert Review of Neurotherapeutics |volume=11 |issue=2 |pages=275–85 |date=February 2011 |pmid=21306214 |pmc=3142267 |doi=10.1586/ern.10.198}}</ref>

People with PTSD have decreased brain activity in the dorsal and rostral [[Anterior cingulate cortex|anterior cingulate]] cortices and the [[ventromedial prefrontal cortex]], areas linked to the experience and regulation of emotion.<ref>{{cite journal |vauthors=Etkin A, Wager TD |title=Functional neuroimaging of anxiety: a meta-analysis of emotional processing in PTSD, social anxiety disorder, and specific phobia |journal=The American Journal of Psychiatry |volume=164 |issue=10 |pages=1476–88 |date=October 2007 |pmid=17898336 |pmc=3318959 |doi=10.1176/appi.ajp.2007.07030504}}</ref>

The amygdala is strongly involved in forming emotional memories, especially fear-related memories. During high stress, the [[hippocampus]], which is associated with placing memories in the correct context of space and time and memory recall, is suppressed. According to one theory, this suppression may be the cause of the [[flashbacks (psychology)|flashbacks]] that can affect people with PTSD. When someone with PTSD undergoes [[stimulus (physiology)|stimuli]] similar to the traumatic event, the body perceives the event as occurring again because the memory was never properly recorded in the person's memory.<ref name="Skelton 2012 628–637" /><ref>{{cite journal |vauthors=van der Kolk B |title=Posttraumatic stress disorder and the nature of trauma |journal=[[Dialogues in Clinical Neuroscience]] |volume=2 |issue=1 |pages=7–22 |date=March 2000 |pmid=22034447 |pmc=3181584 |doi=10.31887/DCNS.2000.2.1/bvdkolk}}</ref>

The amygdalocentric model of PTSD proposes that the amygdala is very much aroused and insufficiently controlled by the medial [[prefrontal cortex]] and the hippocampus, in particular during [[Extinction (psychology)|extinction]].<ref name="Milad">{{cite journal |vauthors=Milad MR, Pitman RK, Ellis CB, Gold AL, Shin LM, Lasko NB, Zeidan MA, Handwerger K, Orr SP, Rauch SL |title=Neurobiological basis of failure to recall extinction memory in posttraumatic stress disorder |journal=[[Biological Psychiatry]] |volume=66 |issue=12 |pages=1075–82 |date=December 2009 |pmid=19748076 |pmc=2787650 |doi=10.1016/j.biopsych.2009.06.026}}</ref> This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability.<ref name="Milad" /><ref name="Stein">{{cite journal |vauthors=Stein MB, Paulus MP |title=Imbalance of approach and avoidance: the yin and yang of anxiety disorders |journal=[[Biological Psychiatry]] |volume=66 |issue=12 |pages=1072–4 |date=December 2009 |pmid=19944792 |pmc=2825567 |doi=10.1016/j.biopsych.2009.09.023}}</ref>

The [[basolateral amygdala|basolateral]] nucleus (BLA) of the amygdala is responsible for the comparison and development of associations between unconditioned and conditioned responses to stimuli, which results in the fear conditioning present in PTSD. The BLA activates the [[central nucleus]] (CeA) of the amygdala, which elaborates the fear response, (including behavioral response to threat and elevated startle response). Descending inhibitory inputs from the [[medial prefrontal cortex]] (mPFC) regulate the transmission from the BLA to the CeA, which is hypothesized to play a role in the extinction of conditioned fear responses.<ref name="Skelton 2012 628–637" />

While as a whole, amygdala hyperactivity is reported by meta analysis of functional neuroimaging in PTSD, there is a large degree of heterogeniety, more so than in social anxiety disorder or phobic disorder. Comparing dorsal (roughly the CeA) and ventral (roughly the BLA) clusters, hyperactivity is more robust in the ventral cluster, while hypoactivity is evident in the dorsal cluster. The distinction may explain the blunted emotions in PTSD (via desensitization in the CeA) as well as the fear related component.<ref>{{cite book |vauthors=Goodkind M, Etkin A |veditors=Sklar P, Buxbaum J, Nestler E, Charney D |title=Neurobiology of Mental Illness |publisher=[[Oxford University Press]] |edition=5th |chapter=Functional Neurocircuitry and Neuroimaging Studies of Anxiety Disorders}}</ref>

In a 2007 study, [[Vietnam War]] combat veterans with PTSD showed a 20% reduction in the volume of their hippocampus compared with veterans who did not have such symptoms.<ref>{{cite book | vauthors = Carlson NR |date=2007 |title=Physiology of Behavior |edition=9th |publisher=[[Pearson Education]]}}</ref> This finding was not replicated in chronic PTSD patients traumatized at an [[Ramstein air show disaster|air show plane crash in 1988]] (Ramstein, Germany).<ref name="Jatzko">{{cite journal |vauthors=Jatzko A, Rothenhöfer S, Schmitt A, Gaser C, Demirakca T, Weber-Fahr W, Wessa M, Magnotta V, Braus DF |title=Hippocampal volume in chronic posttraumatic stress disorder (PTSD): MRI study using two different evaluation methods |journal=[[Journal of Affective Disorders]] |volume=94 |issue=1–3 |pages=121–6 |date=August 2006 |pmid=16701903 |doi=10.1016/j.jad.2006.03.010 |url=http://dbm.neuro.uni-jena.de/pdf-files/Jatzko-JAD06.pdf |archive-url=https://web.archive.org/web/20131019153804/http://dbm.neuro.uni-jena.de/pdf-files/Jatzko-JAD06.pdf |url-status=live |archive-date=2013-10-19}}</ref>

Evidence suggests that endogenous cannabinoid levels are reduced in PTSD, particularly [[anandamide]], and that cannabinoid receptors (CB1) are increased in order to compensate.<ref name="ECS_PTSD">{{cite journal |vauthors=Neumeister A, Seidel J, Ragen BJ, Pietrzak RH |title=Translational evidence for a role of endocannabinoids in the etiology and treatment of posttraumatic stress disorder |journal=[[Psychoneuroendocrinology]] |volume=51 |pages=577–84 |date=January 2015 |pmid=25456347 |pmc=4268027 |doi=10.1016/j.psyneuen.2014.10.012}}</ref> There appears to be a link between increased CB1 receptor availability in the amygdala and abnormal threat processing and hyperarousal, but not dysphoria, in trauma survivors.

A 2020 study found no evidence for conclusions from prior research that suggested low IQ is a risk factor for developing PTSD.<ref>{{Cite journal |vauthors=Shura RD, Epstein EL, Ord AS, Martindale SL, Rowland JA, Brearly TW, Taber KH |date=September 2020 |title=Relationship between intelligence and posttraumatic stress disorder in veterans |journal=Intelligence |language=en |volume=82 |pages=101472 |doi=10.1016/j.intell.2020.101472 |issn=0160-2896 |doi-access=free}}</ref>